Table 4. The HIV-AIDS hypothesis1): 17 predictions versus the facts.

Prediction
Fact
1. Since HIV is "the sole cause of AIDS", it must be abundant in AIDS patients based on "exactly the same criteria as for other viral diseases." But, only antibodies against HIV are found in most patients (1-7)2). Therefore, "HIV infection is identified in blood by detecting antibodies, gene sequences, or viral isolation." But, HIV can only be "isolated" from rare, latently infected lymphocytes that have been cultured for weeks in vitro - away from the antibodies of the human host (8). Thus HIV behaves like a latent passenger virus.
2. Since HIV is "the sole cause of AIDS", there is no AIDS in HIV-free people. But, the AIDS literature has described at least 4621 HIV-free AIDS cases according to one survey - irrespective of, or in agreement with allowances made by the CDC for HIV-free AIDS cases (55).
3. The retrovirus HIV causes immunodeficiency by killing T-cells (1-3). But, retroviruses do not kill cells because they depend on viable cells for the replication of their RNA from viral DNA integrated into cellular DNA (4, 25). Thus, T-cells infected in vitro thrive, and those patented to mass-produce HIV for the detection of HIV antibodies and diagnosis of AIDS are immortal (9-15)!
4. Following "exactly the same criteria as for other viral diseases", HIV causes AIDS by killing more T-cells than the body can replace. Thus T-cells or "CD4 lymphocytes . . . become depleted in people with AIDS". But, even in patients dying from AIDS less than 1 in 500 of the T-cells "that become depleted" are ever infected by HIV (16-20, 54). This rate of infection is the hallmark of a latent passenger virus (21).
5. With an RNA of 9 kilobases, just like polio virus, HIV should be able to cause one specific disease, or no disease if it is a passenger (22). But, HIV is said to be "the sole cause of AIDS", or of 26 different immunodeficiency and non-immunodeficiency diseases, all of which also occur without HIV (table 2). Thus there is not one HIV-specific disease, which is the definition of a passenger virus!
6. All viruses are most pathogenic prior to anti-viral immunity. Therefore, preemptive immunization with Jennerian vaccines is used to protect against all viral diseases since 1798. But, AIDS is observed - by definition - only after anti- HIV immunity is established, a positive HIV/AIDS test (23). Thus HIV cannot cause AIDS by "the same criteria" as conventional viruses.
7. HIV needs "5-10 years" from establishing antiviral immunity to cause AIDS. But, HIV replicates in 1 day, generating over 100 new HIVs per cell (24, 25). Accordingly, HIV is immunogenic, i.e. biochemically most active, within weeks after infection (26, 27). Thus, based on conventional criteria "for other viral diseases", HIV should also cause AIDS within weeks - if it could.
8. "Most people with HIV infection show signs of AIDS within 5-10 years" - the justification for prophylaxis of AIDS with the DNA chain terminator AZT (§ 4). But, of "34.3 million . . . with HIV worldwide" only 1.4% [= 471,457 (obtained by substracting the WHO's cumulative total of 1999 from that of 2000)] developed AIDS in 2000, and similarly low percentages prevailed in all previous years (28). Likewise, in 1985, only 1.2% of the 1 million US citizens with HIV developed AIDS (29, 30). Since an annual incidence of 1.2-1.4% of all 26 AIDS defining diseases combined is no more than the normal mortality in the US and Europe (life expectancy of 75 years), HIV must be a passenger virus.
9. A vaccine against HIV should ("is hoped" to) prevent AIDS - the reason why AIDS researchers try to develop an AIDS vaccine since 1984 (31). But, despite enormous efforts there is no such vaccine to this day (31). Moreover, since AIDS occurs by definition only in the presence of natural antibodies against HIV (§ 3), and since natural antibodies are so effective that no HIV is detectable in AIDS patients (see No. 1), even the hopes for a vaccine are irrational.
10. HIV, like other viruses, survives by transmission from host to host, which is said to be mediated "through sexual contact". But, only 1 in 1000 unprotected sexual contacts transmits HIV (32-34), and only 1 of 275 US citizens is HIV-infected (29, 30), (figure 1b). Therefore, an average uninfected US citizen needs 275,000 random "sexual contacts" to get infected and spread HIV - an unlikely basis for an epidemic!
11. "AIDS spreads by infection" of HIV. But, contrary to the spread of AIDS, there is no "spread" of HIV in the US. In the US HIV infections have remained constant at 1 million from 1985 (29) until now (30), (see also The Durban Declaration and figure 1b). By contrast, AIDS has increased from 1981 until 1992 and has declined ever since (figure 1a).
12. Many of the 3 million people who annually receive blood transfusions in the US for life-threatening diseases (51), should have developed AIDS from HIV-infected blood donors prior to the elimination of HIV from the blood supply in 1985. But there was no increase in AIDS-defining diseases in HIV-positive transfusion recipients in the AIDS era (52), and no AIDS-defining Kaposi's sarcoma has ever been observed in millions of transfusion recipients (53).
13. Doctors are at high risk to contract AIDS from patients, HIV researchers from virus preparations, wives of HIV-positive hemophiliacs from husbands, and prostitutes from clients - particularly since there is no HIV vaccine. But, in the peer-reviewed literature there is not one doctor or nurse who has ever contracted AIDS (not just HIV) from the over 816,000 AIDS patients recorded in the US in 22 years (30). Not one of over ten thousand HIV researchers has contracted AIDS. Wives of hemophiliacs do not get AIDS (35). And there is no AIDS-epidemic in prostitutes (36-38). Thus AIDS is not contagious (39, 40).
14. Viral AIDS - like all viral/microbial epidemics in the past (41-43) - should spread randomly in a population. But, in the US and Europe AIDS is restricted since 1981 to two main risk groups, intravenous drug users and male homosexual drug users (§ 1 and 4).
15. A viral AIDS epidemic should form a classical, bell-shaped chronological curve (41-43), rising exponentially via virus spread and declining exponentially via natural immunity, within months (see figure 3a). But, AIDS has been increasing slowly since 1981 for 12 years and is now declining since 1993 (figure 1a), just like a lifestyle epidemic, as for example lung cancer from smoking (figure 3b).
16. AIDS should be a pediatric epidemic now, because HIV is transmitted "from mother to infant" at rates of 25-50% (44- 49), and because "34.3 million people worldwide" were already infected in 2000. To reduce the high maternal transmission rate HIV-antibody-positive pregnant mothers are treated with AZT for up to 6 months prior to birth (§ 4). But, less than 1% of AIDS in the US and Europe is pediatric (30, 50). Thus HIV must be a passenger virus in newborns.
17. "HIV recognizes no social, political or geographic borders" - just like all other viruses. But, the presumably HIV-caused AIDS epidemics of Africa and of the US and Europe differ both clinically and epidemiologically (§ 1, table 2). The US/European epidemic is highly nonrandom, 80% male and restricted to abnormal risk groups, whereas the African epidemic is random.

1) All quotes are from The Durban Declaration, the most authoritative edition of the HIV-AIDS hypothesis to date, which was signed "by over 5000 people, including Nobel prize winners" and published in Nature in 2000 (The Durban Declaration 2000).

2) Numbers in parentheses are for the following references: (1) (Marx 1984); (2) (Gallo et al 1984); (3) (Altman 1984); (4) (Duesberg 1987); (5) (Duesberg 1988); (6) (Duesberg 1994); (7) (Duesberg and Bialy 1996); (8) (Levy et al 1984); (9) (Hoxie et al 1985); (10) (Anand et al 1987); (11) (Langhoff et al 1989); (12) (Duesberg 1996b); (13) (Weiss 1991); (14) (Cohen 1993); (15) (McCune 2001); (16) (Harper et al 1986); (17) (Schnittman et al 1989); (18) (Hazenberg et al 2000); (19) (Duesberg 1988); (20) (Blattner et al 1988); (21) (Enserink 2001); (22) (Fields 2001); (23) (Centers for Disease Control 1992); (24) (Duesberg and Rasnick 1998); (25) (Duesberg 1992); (26) (Clark et al 1991); (27) (Daar et al 1991); (28) (World Health Organization 2001b); (29) (Curran et al 1985); (30) (Centers for Disease Control and Prevention 2001); (31) (Cohen 2003); (32) (Jacquez et al 1994); (33) (Padian et al 1997); (34) (Gisselquist et al 2002); (35) (Duesberg 1995c; Hoots and Canty 1998); (36) (Mims and White 1984); (37) (Rosenberg and Weiner 1988); (38) (Root-Bernstein 1993); (39) (Hearst and Hulley 1988); (40) (Sande 1986); (41) (Bregman and Langmuir 1990); (42) (Anderson 1996); (43) (Fenner et al 1974); (44) (Blattner et al 1988); (45) (Duesberg 1988); (46) (Blanche et al 1989); (47) (Rogers et al 1989); (48) (European Collaborative Study 1991); (49) (Connor et al 1994); (50) (World Health Organization 2000); (51) (Duesberg 1992); (52) (Ward et al 1989); (53) (Haverkos et al 1994); (54) (Simmonds et al 1990); (55) (Duesberg 1993d).